DOCSLIB.ORG

Diseases of the Immune System 813

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Diseases of the Immune System 813 Chapter 19 | Diseases of the Immune System 813 Chapter 19 Diseases of the Immune System Figure 19.1 Bee stings and other allergens can cause life-threatening, systemic allergic reactions. Sensitive individuals may need to carry an epinephrine auto-injector (e.g., EpiPen) in case of a sting. A bee-sting allergy is an example of an immune response that is harmful to the host rather than protective; epinephrine counteracts the severe drop in blood pressure that can result from the immune response. (credit right: modification of work by Carol Bleistine) Chapter Outline 19.1 Hypersensitivities 19.2 Autoimmune Disorders 19.3 Organ Transplantation and Rejection 19.4 Immunodeficiency 19.5 Cancer Immunobiology and Immunotherapy Introduction An allergic reaction is an immune response to a type of antigen called an allergen. Allergens can be found in many different items, from peanuts and insect stings to latex and some drugs. Unlike other kinds of antigens, allergens are not necessarily associated with pathogenic microbes, and many allergens provoke no immune response at all in most people. Allergic responses vary in severity. Some are mild and localized, like hay fever or hives, but others can result in systemic, life-threatening reactions. Anaphylaxis, for example, is a rapidly developing allergic reaction that can cause a dangerous drop in blood pressure and severe swelling of the throat that may close off the airway. Allergies are just one example of how the immune system—the system normally responsible for preventing disease—can actually cause or mediate disease symptoms. In this chapter, we will further explore allergies and other disorders of the immune system, including hypersensitivity reactions, autoimmune diseases, transplant rejection, and diseases associated with immunodeficiency. 814 Chapter 19 | Diseases of the Immune System 19.1 Hypersensitivities Learning Objectives • Identify and compare the distinguishing characteristics, mechanisms, and major examples of type I, II, III, and IV hypersensitivities In Adaptive Specific Host Defenses, we discussed the mechanisms by which adaptive immune defenses, both humoral and cellular, protect us from infectious diseases. However, these same protective immune defenses can also be responsible for undesirable reactions called hypersensitivity reactions. Hypersensitivity reactions are classified by their immune mechanism. • Type I hypersensitivity reactions involve immunoglobulin E (IgE) antibody against soluble antigen, triggering mast cell degranulation. • Type II hypersensitivity reactions involve IgG and IgM antibodies directed against cellular antigens, leading to cell damage mediated by other immune system effectors. • Type III hypersensitivity reactions involve the interactions of IgG, IgM, and, occasionally, IgA[1] antibodies with antigen to form immune complexes. Accumulation of immune complexes in tissue leads to tissue damage mediated by other immune system effectors. • Type IV hypersensitivity reactions are T-cell–mediated reactions that can involve tissue damage mediated by activated macrophages and cytotoxic T cells. Type I Hypersensitivities When a presensitized individual is exposed to an allergen, it can lead to a rapid immune response that occurs almost immediately. Such a response is called an allergy and is classified as a type I hypersensitivity. Allergens may be seemingly harmless substances such as animal dander, molds, or pollen. Allergens may also be substances considered innately more hazardous, such as insect venom or therapeutic drugs. Food intolerances can also yield allergic reactions as individuals become sensitized to foods such as peanuts or shellfish (Figure 19.2). Regardless of the allergen, the first exposure activates a primary IgE antibody response that sensitizes an individual to type I hypersensitivity reaction upon subsequent exposure. Clinical Focus Part 1 Kerry, a 40-year-old airline pilot, has made an appointment with her primary care physician to discuss a rash that develops whenever she spends time in the sun. As she explains to her physician, it does not seem like sunburn. She is careful not to spend too much time in the sun and she uses sunscreen. Despite these precautions, the rash still appears, manifesting as red, raised patches that get slightly scaly. The rash persists for 7 to 10 days each time, and it seems to largely go away on its own. Lately, the rashes have also begun to appear on her cheeks and above her eyes on either side of her forehead. • Is Kerry right to be concerned, or should she simply be more careful about sun exposure? • Are there conditions that might be brought on by sun exposure that Kerry’s physician should be considering? Jump to the next Clinical Focus box. 1. D.S. Strayer et al (eds). Rubin’s Pathology: Clinicopathologic Foundations of Medicine. 7th ed. 2Philadelphia, PA: Lippincott, Williams & Wilkins, 2014. This OpenStax book is available for free at http://cnx.org/content/col12087/1.4 Chapter 19 | Diseases of the Immune System 815 Figure 19.2 (a) Allergens in plant pollen, shown here in a colorized electron micrograph, may trigger allergic rhinitis or hay fever in sensitive individuals. (b) Skin rashes are often associated with allergic reactions. (c) Peanuts can be eaten safely by most people but can provoke severe allergic reactions in sensitive individuals. For susceptible individuals, a first exposure to an allergen activates a strong TH2 cell response (Figure 19.3). Cytokines interleukin (IL)-4 and IL-13 from the TH2 cells activate B cells specific to the same allergen, resulting in clonal proliferation, differentiation into plasma cells, and antibody-class switch from production of IgM to production of IgE. The fragment crystallizable (Fc) regions of the IgE antibodies bind to specific receptors on the surface of mast cells throughout the body. It is estimated that each mast cell can bind up to 500,000 IgE molecules, with each IgE molecule having two allergen-specific fragment antigen-binding (Fab) sites available for binding allergen on subsequent exposures. By the time this occurs, the allergen is often no longer present and there is no allergic reaction, but the mast cells are primed for a subsequent exposure and the individual is sensitized to the allergen. On subsequent exposure, allergens bind to multiple IgE molecules on mast cells, cross-linking the IgE molecules. Within minutes, this cross-linking of IgE activates the mast cells and triggers degranulation, a reaction in which the contents of the granules in the mast cell are released into the extracellular environment. Preformed components that are released from granules include histamine, serotonin, and bradykinin (Table 19.1). The activated mast cells also release newly formed lipid mediators (leukotrienes and prostaglandins from membrane arachadonic acid metabolism) and cytokines such as tumor necrosis factor (Table 19.2). The chemical mediators released by mast cells collectively cause the inflammation and signs and symptoms associated with type I hypersensitivity reactions. Histamine stimulates mucus secretion in nasal passages and tear formation from lacrimal glands, promoting the runny nose and watery eyes of allergies. Interaction of histamine with nerve endings causes itching and sneezing. The vasodilation caused by several of the mediators can result in hives, headaches, angioedema (swelling that often affects the lips, throat, and tongue), and hypotension (low blood pressure). Bronchiole constriction caused by some of the chemical mediators leads to wheezing, dyspnea (difficulty breathing), coughing, and, in more severe cases, cyanosis (bluish color to the skin or mucous membranes). Vomiting can result from stimulation of the vomiting center in the cerebellum by histamine and serotonin. Histamine can also cause relaxation of intestinal smooth muscles and diarrhea. Selected Preformed Components of Mast Cell Granules Granule Activity Component Heparin Stimulates the generation of bradykinin, which causes increased vascular permeability, vasodilation, bronchiole constriction, and increased mucus secretion Histamine Causes smooth-muscle contraction, increases vascular permeability, increases mucus and tear formation Serotonin Increases vascular permeability, causes vasodilation and smooth-muscle contraction Table 19.1 816 Chapter 19 | Diseases of the Immune System Selected Newly Formed Chemical Mediators of Inflammation and Allergic Response Chemical Activity Mediator Leukotriene Causes smooth-muscle contraction and mucus secretion, increases vascular permeability Prostaglandin Causes smooth-muscle contraction and vasodilation TNF-α (cytokine) Causes inflammation and stimulates cytokine production by other cell types Table 19.2 Figure 19.3 On first exposure to an allergen in a susceptible individual, antigen-presenting cells process and present allergen epitopes with major histocompatibility complex (MHC) II to T helper cells. B cells also process and present the same allergen epitope to TH2 cells, which release cytokines IL-4 and IL-13 to stimulate proliferation and differentiation into IgE-secreting plasma cells. The IgE molecules bind to mast cells with their Fc region, sensitizing the mast cells for activation with subsequent exposure to the allergen. With each subsequent exposure, the allergen cross-links IgE molecules on the mast cells, activating the mast cells and causing the release of preformed chemical mediators from granules (degranulation), as well as newly formed chemical mediators that collectively cause the signs
Load more

Recommended publications
  • IDF Patient & Family Handbook
    Immune Deficiency Foundation Patient & Family Handbook for Primary Immunodeficiency Diseases This book contains general medical information which cannot be applied safely to any individual case. Medical knowledge and practice can change rapidly. Therefore, this book should not be used as a substitute for professional medical advice. FIFTH EDITION COPYRIGHT 1987, 1993, 2001, 2007, 2013 IMMUNE DEFICIENCY FOUNDATION Copyright 2013 by Immune Deficiency Foundation, USA. REPRINT 2015 Readers may redistribute this article to other individuals for non-commercial use, provided that the text, html codes, and this notice remain intact and unaltered in any way. The Immune Deficiency Foundation Patient & Family Handbook may not be resold, reprinted or redistributed for compensation of any kind without prior written permission from the Immune Deficiency Foundation. If you have any questions about permission, please contact: Immune Deficiency Foundation, 110 West Road, Suite 300, Towson, MD 21204, USA; or by telephone at 800-296-4433. Immune Deficiency Foundation Patient & Family Handbook for Primary Immunodeficency Diseases 5th Edition This publication has been made possible through a generous grant from Baxalta Incorporated Immune Deficiency Foundation 110 West Road, Suite 300 Towson, MD 21204 800-296-4433 www.primaryimmune.org [email protected] EDITORS R. Michael Blaese, MD, Executive Editor Francisco A. Bonilla, MD, PhD Immune Deficiency Foundation Boston Children’s Hospital Towson, MD Boston, MA E. Richard Stiehm, MD M. Elizabeth Younger, CPNP, PhD University of California Los Angeles Johns Hopkins Los Angeles, CA Baltimore, MD CONTRIBUTORS Mark Ballow, MD Joseph Bellanti, MD R. Michael Blaese, MD William Blouin, MSN, ARNP, CPNP State University of New York Georgetown University Hospital Immune Deficiency Foundation Miami Children’s Hospital Buffalo, NY Washington, DC Towson, MD Miami, FL Francisco A.
    [Show full text]
  • Vaccination and Autoimmune Disease: What Is the Evidence?
    REVIEW Review Vaccination and autoimmune disease: what is the evidence? David C Wraith, Michel Goldman, Paul-Henri Lambert As many as one in 20 people in Europe and North America have some form of autoimmune disease. These diseases arise in genetically predisposed individuals but require an environmental trigger. Of the many potential environmental factors, infections are the most likely cause. Microbial antigens can induce cross-reactive immune responses against self-antigens, whereas infections can non-specifically enhance their presentation to the immune system. The immune system uses fail-safe mechanisms to suppress infection-associated tissue damage and thus limits autoimmune responses. The association between infection and autoimmune disease has, however, stimulated a debate as to whether such diseases might also be triggered by vaccines. Indeed there are numerous claims and counter claims relating to such a risk. Here we review the mechanisms involved in the induction of autoimmunity and assess the implications for vaccination in human beings. Autoimmune diseases affect about 5% of individuals in Autoimmune disease and infection developed countries.1 Although the prevalence of most Human beings have a highly complex immune system autoimmune diseases is quite low, their individual that evolved from the fairly simple system found in incidence has greatly increased over the past few years, as invertebrates. The so-called innate invertebrate immune documented for type 1 diabetes2,3 and multiple sclerosis.4 system responds non-specifically to infection, does not Several autoimmune disorders arise in individuals in age- involve lymphocytes, and hence does not display groups that are often selected as targets for vaccination memory.
    [Show full text]
  • Early-Phase GVHD Gene Expression Profile in Target Versus Non
    Bone Marrow Transplantation (2013) 48, 284–293 & 2013 Macmillan Publishers Limited All rights reserved 0268-3369/13 www.nature.com/bmt ORIGINAL ARTICLE Early-phase GVHD gene expression profile in target versus non-target tissues: kidney, a possible target? B Sadeghi1, H Al-Chaqmaqchi1, S Al-Hashmi1, D Brodin2, Z Hassan1,3, M Abedi-Valugerdi4, A Moshfegh5 and M Hassan1,3 GVHD is a major complication after allo-SCT. In GVHD, some tissues like liver, intestine and skin are infiltrated by donor T cells while others like muscle are not. The mechanism underlying targeted tropism of donor T cells is not fully understood. In the present study, we aim to explore differences in gene expression profile among target versus non-target tissues in a mouse model of GVHD based on chemotherapy conditioning. Expression levels of JAK–signal transducers and activators of transcription (STAT), CXCL1, ICAM1 and STAT3 were increased in the liver and remained unchanged (or decreased) in the muscle and kidney after conditioning. At the start of GVHD the expression levels of CXCL9, ITGb2, SAA3, MARCO, TLR and VCAM1 were significantly higher in the liver or kidney compared with the muscle of GVHD animals. Moreover, biological processes of inflammatory reactions, leukocyte migration, response to bacterium and chemotaxis followed the same pattern. Our data show that both chemotherapy and allogenicity exclusively induce expression of inflammatory genes in target tissues. Moreover, gene expression profile and histopathological findings in the kidney are similar to those observed in the liver of GVHD mice. Bone Marrow Transplantation (2013) 48, 284–293; doi:10.1038/bmt.2012.120; published online 23 July 2012 Keywords: gene expression; GVHD; kidney; target tissues; mouse model INTRODUCTION none of these reports describe any changes in gene expression Allo-SCT is the treatment of choice for a variety of malignant and profile of non-target tissues like muscle.
    [Show full text]
  • Food Allergy Outline
    Allergy Evaluation-What it all Means & Role of Allergist Sai R. Nimmagadda, M.D.. Associated Allergists and Asthma Specialists Ltd. Clinical Assistant Professor Of Pediatrics Northwestern University Chicago, Illinois Objectives of Presentation • Discuss the different options for allergy evaluation. – Skin tests – Immunocap Testing • Understand the results of Allergy testing in various allergic diseases. • Briefly Understand what an Allergist Does Common Allergic Diseases Seen in the Primary Care Office • Atopic Dermatitis/Eczema • Food Allergy • Allergic Rhinitis • Allergic Asthma • Allergic GI Diseases Factors that Influence Allergies Development and Expression Host Factors Environmental Factors . Genetic Indoor allergens - Atopy Outdoor allergens - Airway hyper Occupational sensitizers responsiveness Tobacco smoke . Gender Air Pollution . Obesity Respiratory Infections Diet © Global Initiative for Asthma Why Perform Allergy Testing? – Confirm Allergens and answer specific questions. • Am I allergic to my dog? • Do I have a milk allergy? • Have I outgrown my allergy? • Do I need medications? • Am I penicillin allergic? • Do I have a bee sting allergy Tests Performed in the Diagnostic Allergy Laboratory • Allergen-specific IgE (over 200 allergen extracts) – Pollen (weeds, grasses, trees), – Epidermal, dust mites, molds, – Foods, – Venoms, – Drugs, – Occupational allergens (e.g., natural rubber latex) • Total Serum IgE (anti-IgE; ABPA) • Multi-allergen screen for IgE antibody Diagnostic Allergy Testing Serological Confirmation of Sensitization History of RAST Testing • RAST (radioallergosorbent test) invented and marketed in 1974 • The suspected allergen is bound to an insoluble material and the patient's serum is added • If the serum contains antibodies to the allergen, those antibodies will bind to the allergen • Radiolabeled anti-human IgE antibody is added where it binds to those IgE antibodies already bound to the insoluble material • The unbound anti-human IgE antibodies are washed away.
    [Show full text]
  • Allergen Regulations 105 Cmr 590.000
    ALLERGEN REGULATIONS 105 CMR 590.000: STATE SANITARY CODE CHAPTER X – MINIMUM SANITATION STANDARDS FOR FOOD ESTABLISHMENTS (1) ADD new definition in 105 CMR 590.002(B): Major Food Allergen means: (1) Milk, eggs, fish (such as bass, flounder, or cod), crustaceans (such as crab, lobster, or shrimp), tree nuts (such as almonds, pecans, or walnuts), wheat, peanuts, and soybeans; and (2) A FOOD ingredient that contains protein derived from a FOOD named in subsection (1). "Major food allergen" does not include: (a) Any highly refined oil derived from a FOOD specified in subsection (1) or any ingredient derived from such highly refined oil; or (b) Any ingredient that is exempt under the petition or notification process specified in the federal Food Allergen Labeling and Consumer Protection Act of 2004 (Public Law 108-282). (2) Amend the definitions of “menu” and “menu board” in 590.002(B) as follows: Menu means a printed list or pictorial display of a food item or items and their price(s) that are available for sale from a food establishment, and includes menus distributed or provided outside of the establishment. Menu Board means any list or pictorial display of a food item or items and their price(s) posted within or outside a food establishment. (3) Amend as follows 105 CMR 590.003(B) (Management and Personnel – federal 1999 Food Code Chapter 2) (B) FC 2-102.11 Demonstration … The areas of knowledge include: . (17) No later than February 1, 2011: (a) Describing FOODS identified as MAJOR FOOD ALLERGENS and describing the symptoms that MAJOR FOOD ALLERGENS could cause in a sensitive individual who has an allergic reaction; and (b) Ensuring that employees are properly trained in food allergy awareness as it relates to their assigned duties.
    [Show full text]
  • Food Allergen Labeling Exemption Petitions and Notifications: Guidance for Industry
    Contains Nonbinding Recommendations Food Allergen Labeling Exemption Petitions and Notifications: Guidance for Industry Additional copies are available from: Office of Food Additive Safety, HFS-205 Center for Food Safety and Applied Nutrition Food and Drug Administration 5001 Campus Drive College Park, MD 20740 (Tel) 240-402-1200 http://www.fda.gov/FoodGuidances You may submit either electronic or written comments regarding this guidance at any time. Submit electronic comments to http://www.regulations.gov. Submit written comments on the guidance to the Division of Dockets Management (HFA-305), Food and Drug Administration, 5630 Fishers Lane, rm. 1061, Rockville, MD 20852. All comments should be identified with the docket number listed in the notice of availability that publishes in the Federal Register. U.S. Department of Health and Human Services Food and Drug Administration Center for Food Safety and Applied Nutrition June 2015 Petitions and Notifications Guidance Page 1 of 18 Contains Nonbinding Recommendations Table of Contents I. Introduction II. Statutory Authority III. Recommendations for Preparing Submissions IV. Additional Information for Petitions V. Additional Information for Notifications VI. Appendices Petitions and Notifications Guidance Page 2 of 18 Contains Nonbinding Recommendations Food Allergen Labeling Exemption Petitions and Notifications Guidance for Industry This guidance represents the Food and Drug Administration’s (FDA’s) current thinking on this topic. It does not create or confer any rights for or on any person and does not operate to bind FDA or the public. You can use an alternative approach if the approach satisfies the requirements of the applicable statutes and regulations. If you want to discuss an alternative approach, contact the FDA staff responsible for implementing this guidance.
    [Show full text]
  • Allergens Immunoglobulin E (Ige) Antibodies
    Allergens − Immunoglobulin E (IgE) Antibodies Single Allergen IgE Antibody This test is principally useful to confirm the allergen specificity in patients with clinically documented allergic disease. Therefore, requests for these tests should be made after a careful and comprehensive medical history is taken. Utilized in this manner, a single allergen immunoglobulin E (IgE) antibody test is cost-effective. A positive result may indicate that allergic signs and symptoms are caused by exposure to the specific allergen. Multi-allergen IgE Antibodies Profile Tests A number of related allergens are grouped together for ordering convenience. Each is tested individually and reported. Sample volume requirements are the same as if the tests were ordered individually. Panel Tests A pooled allergen reagent is used for each panel; therefore, the panel is reported with a single qualitative class result and concentration. The multi-allergen IgE antibody panel, combined with measurement of IgE in serum, is an appropriate first-order test for allergic disease. Positive results indicate the possibility of allergic disease induced by one or more allergens present in the multi-allergen panel. Negative results may rule out allergy, except in rare cases of allergic disease induced by exposure to a single allergen. Panel testing requires less specimen volume and less cost for ruling out allergic response; however, individual (single) allergen responses cannot be identified. In cases of a positive panel test, follow-up testing must be performed to differentiate between individual allergens in the panel. Note: Only 1 result is generated for each panel. Panels may be ordered with or without concurrent measurement of total IgE.
    [Show full text]
  • Anti-Thymocyte Globulin (Atg) and Ciclosporin (Csa)
    Myeloid group ANTI-THYMOCYTE GLOBULIN (ATG) AND CICLOSPORIN (CSA) INDICATION ATG and CSA is indicated for patients who require treatment for aplastic anaemia (AA) but who are not eligible for sibling donor BMT. This includes (note references to severity are based on the modified Camitta criteria): Patients with non-severe aplastic anaemia who are dependent on red cell and/or platelet transfusions. Patients with severe aplastic anaemia (SAA) or very SAA who are > 35-50 years of age. Patients with SAA or very SAA disease who lack an HLA-compatible sibling donor. Protocol may be used in selected patients with hypoplastic marrow conditions. Patients with severe AA who are ≤ 35 years old and have a HLA identical sibling donor, should be treated with allogenic bone marrow transplantation as soon as possible after diagnosis. TREATMENT INTENT Prolong survival Provide a rapid (within 3 months) and sustained improvement in peripheral blood counts Restore haematopoiesis PRE-ASSESSMENT 1. ATG should only used by physicians familiar with administering ATG. Medical and nursing teams must be aware of the side effects and how to treat promptly and appropriately. 2. ATG is highly immunosuppressive - only use in centres with at least level 2 facilities. Patients should be nursed in a single or double isolation room, as an inpatient. 3. Risk of transfusion-associated GvHD following treatment with ATG is unclear, therefore irradiated blood components are currently recommended. It is not known how long the use of irradiated products This is a controlled document and therefore must not be changed Page 1 of 9 ML.2 ATG & CSA Authorised by Myeloid Lead Oct 2019 V.4.1 Prof Adam Mead Myeloid group should be continued, but it may be reasonable to continue while patients are still taking CSA following ATG therapy.
    [Show full text]
  • Allergic Reactions After Vaccination: Translating Guidelines Into Clinical Practice
    R E V I E W EUR ANN ALLERGY CLIN IMMUNOL VOL 51, N 2, 51-61, 2019 A. RADICE1, G. CARLI2, D. MACCHIA1, A. FARSI2 Allergic reactions after vaccination: translating guidelines into clinical practice 1SOS Allergologia e Immunologia, Firenze, Azienda USL Toscana Centro, Italy 2SOS Allergologia e Immunologia, Prato, Azienda USL Toscana Centro, Italy KEYWORDS Summary vaccine; vaccination; allergic reactions; Vaccination represents one of the most powerful medical interventions on global health. anaphylaxis; vaccine hesitancy; vaccine Despite being safe, sustainable, and effective against infectious and in some cases also components; desensitization non-infectious diseases, it’s nowadays facing general opinion’s hesitancy because of a false perceived risk of adverse events. Adverse reactions to vaccines are relatively rare, instead, and those recognizing a hypersensitivity mechanism are even rarer. Corresponding author The purpose of this review is to offer a practical approach to adverse events after vaccina- Anna Radice Ospedale San Giovanni di Dio tion, focusing on immune-mediated reactions with particular regard to their recognition, Via Torregalli 3, 50143 Firenze diagnosis and management. Phone: +39 055 6932304 According to clinical features, we propose an algorythm for allergologic work-up, which E-mail: [email protected] helps in confirming hypersensitivity to vaccine, nonetheless ensuring access to vaccination. Finally, a screening questionnaire is included, providing criteria for immunisation in spe- Doi cialized care settings. 10.23822/EurAnnACI.1764-1489.86 Introduction The gain from vaccination is not just about human health, but it is also a matter of financial resources for health systems. “Smallpox is dead” stated the magazine of the World Health It has been calculated that for every dollar spent in vaccines, Organisation (WHO) in 1980.
    [Show full text]
  • Severe Asthma Associated with Myasthenia Gravis and Upper Airway Obstruction a Souza-Machado,1,2 E Ponte,2 ÁA Cruz2
    Severe Asthma and Myasthenia Gravis CASE REPORT Severe Asthma Associated With Myasthenia Gravis and Upper Airway Obstruction A Souza-Machado,1,2 E Ponte,2 ÁA Cruz2 1Pharmacology Department, Bahia School of Medicine and Public Health, Universidade Federal da Bahia, Salvador–Bahia, Brazil 2Asthma and Allergic Rhinitis Control Program (ProAR), Bahia Faculty of Medicine, Universidade Federal da Bahia, Salvador–Bahia, Brazil ■ Abstract An unusual association of asthma and myasthenia gravis (MG) complicated by tracheal stenosis is reported. The patient was a 35-year-old black woman with a history of severe asthma and rhinitis over 30 years. A respiratory tract infection triggered a life-threatening asthma attack whose treatment required orotracheal intubation and mechanical ventilatory support. A few weeks later, tracheal stenosis was diagnosed. Clinical manifestations of MG presented 3 years after her near-fatal asthma attack. Spirometry showed severe obstruction with no response after inhalation of 400 µg of albuterol. Baseline lung function parameters were forced vital capacity, 3.29 L (105% predicted); forced expiratory volume in 1 second (FEV1), 1.10 L (41% predicted); maximal midexpiratory fl ow rate, 0.81 L/min (26% predicted). FEV1 after administration of albuterol was 0.87 L (32% predicted). The patient’s fl ow–volume loops showed fl attened inspiratory and expiratory limbs, consistent with fi xed extrathoracic airway obstruction. Chest computed tomography scans showed severe concentric reduction of the lumen of the upper thoracic trachea. Key words: Asthma. Tracheal stenosis. Myasthenia gravis. Exacerbation. ■ Resumen En este caso informamos de una asociación infrecuente entre el asma y la miastenia grave (MG) complicada por estenosis traqueal.
    [Show full text]
  • Invasive Aspergillosis Poster IDSA FINAL Pdf.Pdf
    Invasive Aspergillosis Associated with Severe Influenza Infections Nancy Crum-Cianflone MD MPH Scripps Mercy Hospital, San Diego, CA USA Abstract Background (cont.) Results Results (cont.) Background: Bacterial superinfections are well-described complications of influenza • Typically, invasive aspergillosis occurs among severely immunosuppressed hosts Case-Control Study • Systematic Review of the Literature infection, however few data exist on invasive fungal infections in this setting. The Hematologic malignancies, neutropenia, and transplant recipients 48 medical ICU patients underwent influenza testing; 8 were diagnosed with influenza N=52 and present cases (n=5) = 57 total cases • All influenza-positive patients had ventilator-dependent respiratory failure A summary of the cases is shown in Table 2 pathogenesis of invasive aspergillosis may be related to respiratory epithelium • Isolation of Aspergillus sp. in the immunocompetent host without these conditions may be initially considered as a colonizer or non-pathogen Of the 8 patients with severe influenza infection, six (75%) had Aspergillus sp. isolated Increasing number of cases over time: disruption and viral-induced lymphopenia. • 4 A. fumigatus, 1 A. fumigatus and A. versicolor, and 1 A. niger isolated • First cases described in 1979, followed by three cases in the 1980s, two cases in the 1990s, two cases in • However, recent cases have suggested that Aspergillus may rapidly lead to invasive • Since A. niger was of unknown pathogenicity this case was excluded the 2000’s, and 48 cases from 2010 to the 1st quarter of 2016 demonstrating an increasing trend of aspergillosis superinfection (p<0.001) Methods: A retrospective study was conducted among severe influenza cases requiring disease in the setting of severe influenza infection [2,3] Of the 40 patients negative for influenza admitted to the same ICU, none had Aspergillus ICU admission at a large academic hospital (2015-2016).
    [Show full text]
  • ALLERGIC REACTIONS/ANAPHYLAXIS Connie J
    Northwest Community EMS System Paramedic Education Program ALLERGIC REACTIONS/ANAPHYLAXIS Connie J. Mattera, M.S., R.N., EMT-P Reading assignments Text-Vol.1 pp. 235, 1272-1276 SOP: Allergic Reactions/ Anaphylactic Shock Assumed knowledge: Drugs: Epinephrine 1:1,000, 1:10,000; albuterol, ipratropium, dopamine, glucagon KNOWLEDGE OBJECTIVES Upon reading the assigned text assignments and completion of the class and homework questions, each participant will independently do the following with at least an 80% degree of accuracy and no critical errors: 1. Define allergic reaction. 2. Describe the incidence, morbidity and mortality of allergic reactions and anaphylaxis. 3. Identify risk factors that predispose a patient to anaphylaxis. 4. Explain the physiology of the immune system following exposure to an allergen including activation of histamine receptors and the formation of antibodies. 5. Discuss the pathophysiology of allergic reactions and anaphylaxis. 6. Describe the common modes by which allergens enter the body. 7. Compare and contrast natural and acquired and active vs. passive immunity. 8. Identify antigens most frequently associated with anaphylaxis. 9. Differentiate the clinical presentation and severity of risk for a mild, moderate and severe allergic reaction with an emphasis on recognizing an anaphylactic reaction. 10. Integrate the pathophysiologic principles of anaphylaxis with treatment priorities. 11. Sequence care per SOP for patients with mild, moderate and severe allergic reactions. CJM: S14 NWC EMSS Paramedic Education Program ALLERGIC REACTIONS/ANAPHYLAXIS Connie J. Mattera, M.S., R.N., EMT-P I. Immune system A. Principal body system involved in allergic reactions. Others include the cutaneous, cardiovascular, respiratory, nervous, and gastrointestinal systems.
    [Show full text]